Details

Autor(en) / Beteiligte

• Meyer, Christian
• Woerle, Hans J
• Dostou, Jean M
• Welle, Stephen L
• Gerich, John E

Titel

Abnormal renal, hepatic, and muscle glucose metabolism following glucose ingestion in type 2 diabetes

Ist Teil von

• American journal of physiology: endocrinology and metabolism, 2004-12, Vol.287 (6), p.E1049-E1056

Ort / Verlag

United States

Erscheinungsjahr

2004

Quelle

EZB-FREE-00999 freely available EZB journals

Beschreibungen/Notizen

• Departments of 1 Medicine and 2 Physiology and Pharmacology, University of Rochester School of Medicine, Rochester, New York 14642; and 3 Department of Endocrinology, Carl T. Hayden Veterans Affairs Medical Center, Phoenix, Arizona 85012 Submitted 29 January 2004 ; accepted in final form 3 August 2004 Recent studies indicate an important role of the kidney in postprandial glucose homeostasis in normal humans. To determine its role in the abnormal postprandial glucose metabolism in type 2 diabetes mellitus (T2DM), we used a combination of the dual-isotope technique and net balance measurements across kidney and skeletal muscle in 10 subjects with T2DM and 10 age-, weight-, and sex-matched nondiabetic volunteers after ingestion of 75 g of glucose. Over the 4.5-h postprandial period, diabetic subjects had increased mean blood glucose levels (14.1 ± 1.1 vs. 6.2 ± 0.2 mM, P < 0.001) and increased systemic glucose appearance (100.0 ± 6.3 vs. 70.0 ± 3.3 g, P < 0.001). The latter was mainly due to 23 g greater endogenous glucose release (39.8 ± 5.9 vs. 17.0 ± 1.8 g, P < 0.002), since systemic appearance of the ingested glucose was increased by only 7 g (60.2 ± 1.4 vs. 53.0 ± 2.2 g, P < 0.02). Approximately 40% of the diabetic subjects’ increased endogenous glucose release was due to increased renal glucose release (19.6 ± 3.1 vs. 10.6 ± 2.4 g, P < 0.05). Postprandial systemic tissue glucose uptake was also increased in the diabetic subjects (82.3 ± 4.7 vs. 69.8 ± 3.5 g, P < 0.05), and its distribution was altered; renal glucose uptake was increased (21.0 ± 3.5 vs. 9.8 ± 2.3 g, P < 0.03), whereas muscle glucose uptake was normal (18.5 ± 1.8 vs. 25.9 ± 3.3 g, P = 0.16). We conclude that, in T2DM, 1 ) both liver and kidney contribute to postprandial overproduction of glucose, and 2 ) postprandial renal glucose uptake is increased, resulting in a shift in the relative importance of muscle and kidney for glucose disposal. The latter may provide an explanation for the renal glycogen accumulation characteristic of diabetes mellitus as well as a mechanism by which hyperglycemia may lead to diabetic nephropathy. liver; kidney; gluconeogenesis; meal Address for reprint requests and other correspondence: C. Meyer, Carl T. Hayden VA Medical Center, Dept. of Endocrinology, 650 East Indian School Rd., Phoenix, AZ 85012 (E-mail: christian.meyer{at}med.va.gov )